The effect of neural traffic blocking agents on the development of pulmonary platelet trapping associated with traumatic and endotoxin shock will be evaluated. The ability of drugs such as alpha and beta blocking agents, aspirin, and dipyridamole to reduce the extent of pulmonary platelet trapping associated with these insults will be assessed. The effect of intimal dissection on adhesion and aggregation will be defined using major blood vessels of the extremity. In veins of the extremities the importance of the vasovasorum and local trauma on the evolution of platelet aggregates will be determined, and will provide a potential for drug therapy in deep venous thrombosis and pulmonary embolization. The effects of a low-flow state on intravascular platelet aggregation will also be assessed. Using a "lost-wax" technique luminal cast models from various parts of the circulation will be studied. The geometry of these models in the normal flow state and following the induction of shock will be assessed and the hemodynamics studied.